A Review of PediatricIdiopathic Intracranial

Hypertension

David L. Rogers, MD

KEYWORDS

� Pediatric idiopathic intracranial hypertension � Pseudotumor cerebri � Papilledema

KEY POINTS

� Many children who suffer with headaches first present to their pediatrician for evaluation.Intracranial hypertension must be included in the differential diagnosis. Missing the diag-nosis could result in permanent and severe visual loss.

� Idiopathic intracranial hypertension occurs in both children and adults.

� Making the diagnosis of idiopathic intracranial hypertension in a child can now be donewith more confidence because of newly outlined diagnostic criteria.

� A significant percentage of pediatric patients with intracranial hypertension will have anidentifiable secondary cause.

� Most children diagnosed with idiopathic intracranial hypertension will respond well tomedical management alone.

� Surgical intervention is reserved for those who fail to respond medically.

INTRODUCTION

Idiopathic intracranial hypertension (IIH) is defined as elevated intracranial pressure(ICP) without clinical, radiologic, or laboratory evidence of a secondary cause. Themost frequently cited incidence data for IIH in the general population of the UnitedStates are from a study by Durcan and colleagues,1 who reported the incidence tobe 1 in 100,000 individuals. When restricting the inclusion criteria to women aged20 to 44 years, who are 20% or more above their ideal body weight, the annual inci-dence increases to 15 to 19 cases per 100,000 in the United States.1 Although it hashistorically been described as a condition affecting obese women of childbearing age,it can occur in all age groups and genders in both obese and nonobese individuals andis becoming more recognized in the pediatric population.

Financial Conflict of Interest by Author: None.Department of Ophthalmology, Nationwide Children’s Hospital, The Ohio State University Col-lege of Medicine, 555 South 18th Street, Suite 4C, Columbus, OH 43205, USAE-mail address: David.Rogers@nationwidechildrens.org

Pediatr Clin N Am 61 (2014) 579–590http://dx.doi.org/10.1016/j.pcl.2014.03.004 pediatric.theclinics.com0031-3955/14/$ – see front matter � 2014 Elsevier Inc. All rights reserved.

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NOMENCLATURE

There has been much discussion and debate about the appropriate nomenclature todescribe this condition. Historically, the condition has been referred to by termssuch as meningitis serosa,2 otitic hydrocephalus,3 hypertensive meningeal hydrops,4

pseudotumor cerebri,5 benign intracranial hypertension,6 idiopathic intracranial hyper-tension,7 and, most recently, pseudotumor cerebri syndrome.8 With so many names,confusion and misunderstanding can occur. The more descriptive term “intracranialhypertension,” which is then further classified as either “idiopathic” or “secondary,”is used in this discussion. The term “idiopathic” is reserved for those cases in whichknown secondary causes have been excluded. The term “secondary” is used for thosecases in which an underlying cause is identified. These terms are simple, descriptive,and understood by all clinicians. It is important to recognize that little is known aboutthe pathophysiology of IIH. It is quite possible that what is referred to today as “idio-pathic” may likely become “secondary” as more is learned about the disease process.

DEMOGRAPHICS

More information is becoming available regarding the demographics of pediatric IIH.Current data suggest that prepubertal children affected with intracranial hypertensionare more likely to be secondary rather than idiopathic in nature. In addition, the asso-ciation with obesity and female gender does not hold true in this population.9,10

Studies also suggest that IIH is infrequent in children less than 10 years of age9 andextremely rare in infants less than 3 years old.

ASSOCIATED CONDITIONS

There are a myriad of secondary causes of intracranial hypertension and knowledge ofthese associated conditions will aid the clinician during the history and examination ofthe patient and can assist in guiding the subsequent workup. It is worth mentioningagain that pediatric intracranial hypertension is more likely to be secondary in naturethan idiopathic. Systemic conditions, cerebral venous abnormalities, drugs, endocrineabnormalities, and infectious causes have been identified as secondary causes ofintracranial hypertension in the literature (Box 1). The exact mechanism by whichthese conditions result in secondary intracranial hypertension is not entirely under-stood in all cases.

CLINICAL PRESENTATION

The clinical presentation of pediatric IIH includes many of the same symptoms andobjective findings as the adult patient. Headache is by far the most common symptomof IIH and occurs in more than 90% of cases.11 There is no specific headache patternthat is pathognomonic of IIH; therefore, a thorough history and physical examinationare needed to try and determine the need for further evaluation. Other symptomsinclude neck, shoulder, or arm pain, nausea, vomiting, pulsatile tinnitus, diplopia,blurred vision, and transient obscurations of vision.12,13 Diplopia can be secondaryto unilateral or bilateral sixth nerve palsies. The sixth cranial nerve is susceptible todamage from high ICP alone. Infrequently, patients may present with no suggestivesymptoms at all and are only diagnosed when papilledema identified on routine eyeexamination prompts a further workup. For example, a thin 14-year-old girl presentedfor her regular eye examination and was found to have papilledema. She had beenstarted on clindamycin for acne 8 weeks previously. Only retrospectively when prod-ded did she complain of new headaches. Within 2 weeks of stopping the clindamycin,

Box 1

Secondary causes and conditions associated with intracranial hypertension

Medical and Systemic Conditions Infectious Diseases Drugs

Head trauma

Subarachnoid hemorrhage

Decreased CSF absorption from priorintracranial infection or hemorrhage

Cerebral venous abnormalities

Bilateral jugular vein thrombosis orsurgical ligation

Increased right heart pressure

Arteriovenous fistulas

Superior vena cava syndrome

Hypercoagulable states

Renal failure

Liver failure

Sleep apnea

Cystinosis

Lupus

Sarcoidosis

Hypoparathyroidism

Addison disease

Behcet disease

Middle ear or mastoid infection

Hypercapnia

Pickwickian syndrome

Anemia

Turner syndrome

Down syndrome

Bacterial and viral meningitis

Lyme disease

Human immunodeficiencyvirus

Poliomyelitis

Coxsackie B viral encephalitis

Guillain-Barre syndrome

Infectious mononucleosis

Syphilis

Malaria

Tetracycline

Minocycline

Doxycycline

Nalidixic acid

Sulfa drugs

Vitamin A

Isotretinoin

All-trans-retinoic acid

Amiodarone

Nitofurantoin

Lithium

Levonorgestrel

Growth hormone

Thyroxine

Leuprorelin acetate

Steroid withdrawal

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all signs and symptoms resolved. Many children with refractive errors have experi-enced headaches when their glasses need updated, and it is possible for childrento attribute blurry vision and headaches to the need for new glasses. This type ofheadache should be intermittent and mild.

EVALUATION

A thorough history is imperative when assessing a child with IIH. Both the parent andthe child should be involved when the history is obtained, because the child’s inputcan be a source of valuable information. The history should be focused on clarifyingthe patient’s symptoms and identifying potential secondary causes. Demographic in-formation should include the child’s age, gender, and weight. Specific questioningshould address stage of puberty, recent illnesses, medication use, recent weight

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gain, headache, nausea, vomiting, neck and back pain, systemic illnesses, and otherneurologic complaints.The clinical examination should focus on identifying features of IIH. Neurologic

and ophthalmologic assessments are indicated. The ophthalmologic evaluation inthe pediatrician’s office should include a vision test, extraocular motility evaluation(specifically looking for abduction deficits that might indicate the presence of sixthnerve involvement), pupil evaluation, and examination of the optic nerve with adirect ophthalmoscope. The presence of disc edema in an undilated pupil can bevery difficult to evaluate especially if it is very mild (Fig. 1). Moderate papilledema(Fig. 2) and florid papilledema (Fig. 3) are more obvious and can be accompaniedby retinal hemorrhages and cotton wool spots. Pseudopapilledema can be causedby the presence of drusen buried in the nerve head (Fig. 4). Even if the nerves looknormal (Fig. 5), this should not preclude referral to a pediatric ophthalmologistbecause the appearance might be evolving or disc edema could be absent. Evalu-ating the nerves and seeing any evidence of disc edema help the pediatrician makethe referral emergent. The neurologic examination should be directed at identifyingany focal neurologic deficits. If referral is warranted, the ophthalmic examinationshould be performed by an ophthalmologist familiar with the condition. The detailedexamination should include assessing visual acuity, color vision, visual fields, extra-ocular movements, and a careful anatomic evaluation. Papilledema is the mostimportant clinical finding because it is associated with vision loss, the most fearedconsequence of IIH. Photographs of the optic nerve are taken for monitoring pur-poses. The role of optical coherence tomography (OCT) in identifying and moni-toring papilledema is not yet clear. The author currently performs this test onevery patient and has found it to be a useful tool for monitoring response to treat-ment. OCT is a noninvasive imaging test that uses light to measure different layersin the retina and optic nerve. OCT is proven to be helpful in other ocular diseases,including glaucoma, diabetic retinopathy, and macular degeneration. If studiesconfirm that OCT is accurate and reliable in evaluating the response to treatmentin patients with IIH, it will help decrease the number of lumbar punctures (LPs) per-formed on children with IIH.

Fig. 1. Presence of disc edema in an undilated pupil.

Fig. 2. Moderate papilledema.

Fig. 3. Florid papilledema.

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Fig. 4. Pseudopapilledema caused by the presence of drusen buried in the nerve head.

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DIAGNOSTIC CRITERIA

Dandy14 first presented diagnostic criteria for IIH without brain tumor in 1937. Inadults, modified criteria are now used.15 As previously mentioned, the pediatric pa-tient with IIH is much different than the typical adult counterpart. Pediatricians and pe-diatric subspecialists familiar with these criteria frequently struggle to apply them inthe pediatric population. The challenge of diagnosing pediatric IIH was recentlyaddressed by Friedman and colleagues.16 They proposed a modified criteria thatinclude specific recommendations for determining if cerebrospinal fluid (CSF) openingpressure is elevated, one of themost difficult issues in the pediatric population (Box 2).These newly proposed criteria are comprehensive and also address an increasinglymore common issue of diagnosing IIH in children without papilledema. Cliniciansshould be cautioned against empirically dismissing the diagnosis of IIH in pediatric

Fig. 5. Normal optic disc appearance.

Box 2

Diagnostic criteria for IIH

1. Required for diagnosis of IIH

A. Papilledema

B. Normal neurologic examination except for cranial nerve abnormalities

C. Neuroimaging: normal brain parenchyma without evidence of hydrocephalus, mass, orstructural lesion and no abnormal meningeal enhancement on MRI, with and withoutgadolinium, for typical patients (female and obese), and MRI, with and withoutgadolinium, and magnetic resonance venography for others; if MRI is unavailable orcontraindicated, contrast-enhanced CT may be used

D. Normal CSF composition

E. Elevated LPOP (�250 mm CSF in adults and �280 mm CSF in children [250 mm CSF if thechild is not sedated and not obese]) in a properly performed LP

2. Diagnosis of IIH without papilledema

In the absence of papilledema, a diagnosis of IIH can be made if B–E from above are satisfied,and in addition, the patient has a unilateral or bilateral abducens nerve palsy

In the absence of papilledema or sixth nerve palsy, a diagnosis of IIH can be suggested but notmade if B–E from above are satisfied, and in addition, at least 3 of the following neuroimagingcriteria are satisfied:

i. Empty sella

ii. Flattening of the posterior aspect of the globe

iii. Distention of the perioptic subarachnoid space with or without a tortuous optic nerve

iv. Transverse venous sinus stenosis

A diagnosis of IIH is definite if the patient fulfills criteria A–E.

The diagnosis is considered probable if criteria A–D are met but the measured CSF pressure islower than specified for a definite diagnosis.

Adapted from Friedman DI, Liu GT, Digre KB. Revised diagnostic criteria for the pseudotumorcerebri syndrome in adults and children. Neurology 2013;81:1159–65.

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patients without papilledema and should use the diagnostic category “probable IIH”proposed by Friedman and colleagues in these patients.

WORKUP

If intracranial hypertension is suspected, the subsequent workup should be done assoon as possible. Initial neuroimaging, usually with computed tomographic (CT)scan, should be performed and, if unremarkable, an LP with opening pressure shouldbe performed. Further workup should be directed to rule out secondary causes andshould be guided by the history and examination findings. Therefore, the workup ofany individual patient is unique. The following is therefore offered as a guide andshould not be considered a comprehensive assessment approach. When an initialworkup suggests possible IIH, urgent neurologic and ophthalmologic evaluationsare mandatory. Other testing to rule out secondary causes should be guided by thehistory and physical findings.The LP can be difficult to obtain in a child who is awake. Many times this test must

be performed under sedation. The preferred positioning is in the lateral decubitus po-sition. Measuring the opening pressure should be done routinely. CSF should be

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removed and sent for appropriate diagnostic testing. In general, a basic cell count andcultures are done with the addition of other tests as directed by the clinical history andexamination. The CSF composition should be normal.Interpreting results of lumbar puncture opening pressure (LPOP) in the pediatric

population is difficult because of the lack of any large-scale normative data. However,there is growing evidence in the literature that can guide the clinician in interpretingthese results. Current evidence suggests that the upper limit of normal for LPOP inchildren between 1 and 18 years of age is 280 mm H2O,17–19 whereas neonateshave a lower threshold set at 76mmH2O.20 However, these studies have small samplesizes, and guidelines based on age alone are problematic. One of the problems thiscreates is dealing with the ends of the spectrum, such as the 18 year old with LPOPthat is considered normal at 270 mm H2O but would be abnormal if at 19 years ofage. An LPOP greater than 280 mm H2O is clearly abnormal with or without papille-dema. The author also considers an LPOP of 250 mm H2O as being abnormal if pap-illedema is present in conjunction with other clinical signs, and symptoms areconsistent with IIH.Neuroimaging is required before a diagnosis of IIH can be made. In some cases, the

initial workup for IIH is done as soon as possible because of the acute onset of symp-toms. In this setting, a CT scan is usually done before performing an LP to rule outintracranial pathologic abnormality. A normal CT scan of the brain is never adequatein making the diagnosis of IIH. Magnetic resonance imaging (MRI) of the brain with andwithout gadolinium and MR venography are the studies of choice to rule out knownsecondary causes.21

To make the diagnosis of IIH, neuroimaging should demonstrate normal brainparenchyma without evidence of hydrocephalus, mass, or structural lesion and noabnormal meningeal enhancement.16 However, several abnormal MRI findings havebeen reported. Some of these include empty sella, partially empty sella/decreasedpituitary height, flattened posterior glove/sclera, enlarged optic nerve sheath diam-eter, increased tortuosity of the optic nerve, enhancement of the optic nerve, intraoc-ular protrusion of the optic nerve, and slitlike ventricles. Flattening of the posterioraspect of the globe, protrusion of the optic nerve into the intraocular space, and slitlikeventricles are highly specific for intracranial hypertension.22–25

TREATMENT

The best approach to managing IIH is with a multidisciplinary team that at minimumincludes a neurologist and an ophthalmologist. Other specialists such as a hematolo-gist, nutritionist, and endocrinologist can be called on as needed. A good working rela-tionship among these specialists is essential. For simplicity, designating one specialistto manage all aspects of pharmacologic treatment will prevent confusion to the pa-tient, parents, and other members of the medical team. The neurologist is the ideal in-dividual for this task. The ophthalmologist works closely with the neurologist to guidetreatment based on the ophthalmic findings, whereas the neurologist manages themedications and monitors for systemic side effects and other issues.Randomized clinical trials are lacking in the pediatric population and the treatment

of IIH is largely based on evidence obtained in the adult population. Lowering ICP isthe mainstay of treatment with a purpose of preserving vision and controlling symp-toms. However, identifying and directing treatment at the underlying cause cannotbe overemphasized. In general, medical management is used first and surgical treat-ment is reserved for cases in which medical therapy fails to control ICP or if visualfunction is threatened.

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Weight loss should not be neglected in patients who are overweight. One case se-ries showed that a weight reduction of 6% can result in a reversal of papilledema.26

Another study of obese women with IIH showed that weight loss effectively reducesnot only headaches and papilledema, but also ICP.27 Fortunately, most cases of pe-diatric IIH will respond well to treatment; however, a small percentage will havesome degree of permanent visual loss.28–30

EMERGENT TREATMENT

Initial treatment is aimed at lowering ICP and preserving visual function. In caseswhere visual function is threatened because of severe papilledema, emergent neuro-surgical CSF diversion may be required. However, medical management should notbe delayed. A short course of high-dose oral or intravenous steroids can be used inaddition to either oral or intravenous acetazolamide. The patient should be monitoredclinically for signs of deterioration in visual function. Optic nerve sheath fenestration(ONSF) is typically reserved for cases wherein acute elevation of ICP would threatenvisual function and to protect the optic nerve from further injury in recurrent cases.The ONSF should not be used as a long-term means of lowering ICP or as a treatmentof headaches.

PHARMACOLOGIC TREATMENT

Carbonic anhydrase inhibitors have been shown to decrease ICP and treat papille-dema.31 Acetazolamide is the most commonly used carbonic anhydrase inhibitor.Furosemide is usually reserved for cases in which acetazolamide is not toleratedbecause of its minimal effect on lowering ICP. Topiramate is an antiepileptic drugwith the secondary effect of inhibiting carbonic anhydrase. It has been used as analternative to acetazolamide and has the added benefit of suppressing appetite, mak-ing it a good choice for those patients who are obese. The role of corticosteroids hasnot been proven; however, the author uses a short course of high-dose corticosteroidsfor acute cases of elevated ICP and papilledema associated with acute vision loss.

SURGICAL TREATMENT

The 2 surgical approaches used in the management of IIH are CSF shunting proce-dures and ONSF. In 1873, de Wecker32 introduced the ONSF. It is used to treat pap-illedema that is unresponsive to medical management. Most patients have resolutionof papilledema and stabilization of vision with this procedure.33,34 From a vascularperspective, the optic nerve head is a delicate area described as a watershed. CSFpressure at the optic nerve head is thought to cause papilledema. The ONSF likelyworks by inducing a circumferential scar to form between the optic nerve sheathand the optic nerve directly behind the globe, effectively redirecting the pressurehead of CSF from the optic nerve head and moving it posteriorly to an area that ismore resilient. This theory is supported by the fact that ICP remains elevated afterONSF and that the fenestration itself scar down and does not remain open overtime.35–39 This simple explanation does not entirely explain the mechanism by whichthe ONSF works, as there are reports of patients who have had unilateral ONSF thatresulted in a resolution of papilledema in the fellow eye and improvement inheadache.33,34,40,41

There are several CSF shunting options but the 2 most frequently used approachesare lumboperitoneal shunt and ventriculoperitoneal shunt. It is the author’s experienceas well as the experience of others that lumboperitoneal shunting is the most effective

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approach for treating papilledema and alleviating symptoms.35 Serial LP continues tobe used to treat IIH. In some cases LPs are performed weekly or biweekly. In the au-thor’s experience, this is a poor treatment option because it has no long-term benefit,is painful for the child, worsens anxiety, is difficult in obese patients, and may requirefrequent sedation. LP is reserved for initial diagnostic purposes and subsequently onlywhen needed to monitor CSF pressure in response to treatment.

SUMMARY

The diagnosis of IIH in a pediatric patient is becoming more common. Themost impor-tant first step is including IIH in the differential diagnosis of any child with new-onset orchronic headaches. Understanding of the diagnosis and treatment of this condition haslargely been based on data obtained in the adult population. Now a growing body ofevidence demonstrates that pediatric IIH is quite different than the adult disease. Anincreased understanding of how this disease affects children has led to more specificdiagnostic and treatment guidelines that will aid the clinician in treating these patients.

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